Neuroinflammation is associated with Alzheimer's disease (AD) pathology (Chen, K. et al., 281 Peptide J. Biol. Chem. 3651-59 (2006) and Frenkel, D. et al., 115 J. Clin. Inves. 2423-33 (2005)). Neuroinflammation involves an accumulation of a large number of activated microglia and astrocytes as well as small numbers of T cells, mostly adhering to postcapillary venules (Agadjanyan, M. G. et al., 174 J. Immunol. 1580-86 (2005); Dickson, D. et al., 7 Glia 75-83 (1993); and Fillit, H. et al., 129 Neurosci. Lett. 318-20 (1991)). Both microglia and astrocytes have been shown to generate β-amyloid protein (Aβ), one of the main pathologic features of AD. Aβ itself has been shown to act as a pro-inflammatory agent causing the activation of many inflammatory components. Accompanying biochemical alterations include the appearance or up-regulation of numerous molecules characteristic of inflammation and free radical attack. Particularly important may be the complement proteins, acute phase reactants and inflammatory cytokines. Patients that take non-steroidal anti-inflammatory drugs have a lower risk of AD than those who do not. These results have led to increased interest in pursuing anti-inflammatory therapy for AD (Fillit, H. 1991).